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The mechanisms by which cells respond to their changing mechanical environment and how this stimulus is decoded intracellularly from the tissue to the organ level, are widely considered as fundamental for most biological processes. Despite this, the underlying phenomena of mechanotransduction, are still not very well understood. Over the last years, numerical modeling has emerged as a cohesive element in the interpretation of biophysical and biochemical assays, concerning cellular mechanotransduction. We hypothesize that the consideration of continuum mechanics (studying all cellular entities as solids) is an inherent limitation of these models, and in part, responsible for their restricted application in cellular biomechanics. To evaluate this, a (verified and validated) 3D model of osteoblast is simulated through structural analysis, employing conventional Finite Element (FE) modelling and the results compared to a Fluid-Structure Interaction (FSI) analysis. Among the trend observed, FSI systematically leads to a higher stimulation of the nucleus (by up to 200%), while FE produced a more uniform stress field, resulting in the deformation of a notably larger portion of its volume. Although FE modelling captures a seemingly correct kinematic response of the cell when subjected to the simulated loading scenario, FSI represents a more realistic alternative. The equitable consideration of both, liquid- and solid-state material characteristics, in the latter analysis, revealed intra-cellular loading patterns that were more realistic from a biomechanical perspective. In conclusion, FSI can provide refined insight as to nuclear loading, thus serving as a far more accurate framework for decoding cellular mechanotransduction. |
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